乳腺癌组织COX-2、VEGF-C的表达与淋巴结转移的关系

Correlation of COX-2 and VEGF-C expressions in breast carcinoma with lymph node metastasis

目的研究COX-2、VEGF-C在乳腺癌组织中的表达及其与淋巴管生成、淋巴结转移间的相关性。方法采用免疫组化学S-P法检测46例浸润性导管癌组织中COX-2、VEGF-C的表达,通过淋巴管特异性标记物D2-40记数淋巴管密度(LVD),分析COX-2、VEGF-C的表达与淋巴管生成和淋巴结癌组织转移的相关性。结果①乳腺癌组织COX-2、VEGF-C表达阳性率分别为73.91%(34/46)和71.74%(33/46)。②有淋巴结转移组COX-2阳性率为86.48%(32/37)、VEGF-C为81.08%(30/37),D2-40阳性淋巴管密度为(13.350±3.097)/×200。无淋巴结转移组COX-2为22.22%(2/9)、VEGF-C为33.33%(3/9)、LVD为(9.560±2.031)/×200,转移组中COX-2、VEGF-C的表达及淋巴管密度均明显高于无转移组(P<0.01)。③VEGF-C表达与COX-2表达呈正相关(r=0.757,P<0.01),并且COX-2、VEGF-C的表达与LVD也呈正相关(P<0.01)。结论VEGF-C、COX-2在人乳腺癌组织呈高水平表达,其表达与肿瘤淋巴管密度及癌组织淋巴结转移有关;COX-2可能通过诱导VEGF-C表达促进肿瘤淋巴管生成和淋巴结转移。

Objective To investigate the expressions of COX-2 and VEGF-C in breast carcinoma and their correlation with lymphangiogenesis and lymph node metastasis. Methods The expressions of COX-2 and VEGF-C and D2-40 were evaluated in 46 cases of breast carcinoma by immunohistochemical staining SP methods. The lymphatic vessels density （LVD） in tumor was counted through the special marker D2-40. Results The positive rate of COX-2 and of VEGF-C was 73.91% （34/46） and 71.74% （33/46） respectively in breast carcinoma tissues. The positive rate of COX-2 and VEGF-C was 86.48% （32/37） and 81.08% （30/37）, and LVD was （13. 350 ±3. 097）/×200 in the lymph node metastasis group, while that in non-lymph-node metastasis group was 22.22% （2/9）, 33.33% （3/9） and （9. 560 ± 2. 031 ）/× 200 respectively, with significant difference between the two groups （P 〈 0.01 ）. VEGF-C expression was positively correlated with COX-2 expression （r = 0. 757, P 〈 0. 01 ）. The expressions of COX-2 and VEGF-C were positively correlated with LVD （P 〈 0. 01 ）. Conclusion The expressions of COX-2 and VEGF-C were high in breast carcinoma, which were closely related with tumor LVD and lymph node metastasis. A positive correlation was found between the expressions of VEGF-C and COX-2 in breast carcinoma. COX-2 may promote tumor lymphangiogenesis and metastasis of tumor lymph node by inducing VEGF-C expression.